Dartmouth Medical School - Faculty Database

Title(s):
Dean of Dartmouth Medical School
Chair and Professor of Microbiology and Immunology

Department(s):
Microbiology and Immunology

Education:
Case Western Reserve University, PHD 1977
University of Michigan, BS 1972

His subsequent postdoctoral work was supported by an individual NIH postdoctoral fellowship, and he was a research associate in Immunology at first Johns Hopkins University School of Medicine and then at the Fred Hutchinson Cancer Research Center (FHCRC) and the University of Washington (UW) in Seattle. He became an Assistant Member/Professor at FHCRC and the UW in 1980. Dr. Green joined the faculty of the Department of Microbiology at Dartmouth Medical School in 1983. From 1992-2002 Dr. Green served as Director of the Immunology Program, including the Immunology and Cancer Immunotherapy Program of the Norris Cotton Cancer Center, before becoming Chair of the Microbiology and Immunology Department in July, 2002.

Programs:
Immunology Program
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
Program in Experimental and Molecular Medicine

Websites:
http://dms.dartmouth.edu/microbio/
http://dms.dartmouth.edu/immuno/
http://www.dartmouth.edu/~mcb/
http://dms.dartmouth.edu/COBRE/
http://dms.dartmouth.edu/dean/green/

T Cell Immune Responses to Retroviral Diseases

The primary interests of the lab focus on cell-mediated immunity to mouse retroviruses that cause either leukemia or immunodeficiency. We have been studying resistance to endogenous AKR/Gross virus-induced leukemia mediated by cytotoxic T lymphocyte (CTL) responses. By use of "low leukemia" mouse strains, CTL that readily lyse AKR/Gross retrovirus-induced tumors have been generated. The CTL recognize "type-specific" viral determinants with the major immunodominant viral peptide located in the transmembrane anchor protein encoded by the envelope gene. Other mouse strains of higher leukemia incidence are unable to generate such CTL responses. The mechanism of unresponsiveness include both MHC-dependent mechanisms and apoptosis of effector CTL following interaction with FasL-expressing virus infected cells.

Another area of emphasis is the study of both immunity to the mouse acquired immunodeficiency syndrome (MAIDS) retroviral isolate and the mechanism of retroviral pathogenesis. In this model of HIV induced AIDS, we have raised unique protective CTL to the causative virus. Interestingly, the immunodominant determinant recognized by the CTL is encoded by a previously unrecognized alternative viral translational reading frame. Moreover, this alternative reading frame is extended, and mutagenesis experiments have shown that it exists because its protein product is necessary for viral pathogenesis. We are also interested in novel vaccine approaches, particularly to the Category A biodefense agent, smallpox virus.